Prostate cancer represents a significant health care burden and is the second leading cause of cancer-related mortality in men. See Siegel, R.; Ma, J.; Zou, Z.; Jemal, A. CA Cancer J. Clin. 2014, 64, 9. Among the challenges in this area is the problem of recurrent prostate cancer following androgen-deprivation therapy (i.e., castration). Medical castration initially depletes androgens such as testosterone and its reduced form, 5α-dihydrotestosterone. However, the cancer inevitably reoccurs, and a previously unappreciated but sinister backdoor pathway (Fiandalo, M. V.; Wilton, J.; Mohler, J. L. Int. J. Biol. Sci. 2014, 10, 596) converts an intermediate in cholesterol metabolism, 17α-hydroprogesterone first to 4-androstene-3,17-dione and then to dihydrotestosterone without passing through testosterone. Accordingly, there is a continuing need to develop therapies to reduce the elevated levels of these androgens as a means to treat recurrent prostate cancer.